甲型流感病毒刺激鼻上皮细胞表达嗜酸性粒细胞趋化因子。

Influenza virus A stimulates expression of eotaxin by nasal epithelial cells.

作者信息

Kawaguchi M, Kokubu F, Kuga H, Tomita T, Matsukura S, Suzaki H, Huang S K, Adachi M

机构信息

First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.

出版信息

Clin Exp Allergy. 2001 Jun;31(6):873-80. doi: 10.1046/j.1365-2222.2001.01103.x.

DOI:10.1046/j.1365-2222.2001.01103.x

PMID:11422151

Abstract

BACKGROUND

Respiratory virus is one of the most common causes of airway inflammation, but its pathogenic mechanisms are not well understood. Eotaxin is a potent eosinophil chemoattractant and is a selective agonist for C-C chemokine receptor 3 (CCR3). Although it has recently been demonstrated that epithelial cells express eotaxin, both in vivo and in vitro, there are few data concerning the expression in viral infection.

OBJECTS

We hypothesized that eotaxin may play an important role in attracting inflammatory cells into the airway after viral infection and analysed whether viral infection induces eotaxin in nasal epithelial cells in vitro.

METHODS

Nasal epithelial cells obtained from polypectomy for nasal polyp were infected with influenza virus A (subtype H3N2). The cells and supernatants were collected 8, 24 and 48 h after infection. Eotaxin mRNA was analysed by RT-PCR. Eotaxin concentration in the supernatants was analysed by enzyme-linked immunosorbent assay. We also examined a blocking assay to analyse the intervention of pro-inflammatory cytokines, TNF-alpha and IL-1beta in eotaxin production induced by influenza virus.

RESULTS

The results showed that eotaxin was expressed constitutively in uninfected cells, but was up-regulated for both mRNA and protein levels in infected cells. Blocking experiments using anti-TNF-alpha and anti-IL-1beta antibodies showed no effects of these agents on the level of eotaxin. In addition, UV-inactivated virus did not enhance the expression of eotaxin.

CONCLUSIONS

These results suggest that influenza virus A infection in nasal epithelial cells stimulates the expression of eotaxin, and may play an important role in the pathogenesis of airway inflammation by inducing eotaxin.

摘要

背景

呼吸道病毒是气道炎症最常见的病因之一，但其致病机制尚未完全明确。嗜酸性粒细胞趋化因子是一种有效的嗜酸性粒细胞趋化剂，是C-C趋化因子受体3（CCR3）的选择性激动剂。尽管最近已证实在体内和体外上皮细胞均表达嗜酸性粒细胞趋化因子，但关于病毒感染时其表达的资料较少。

目的

我们推测嗜酸性粒细胞趋化因子在病毒感染后吸引炎性细胞进入气道中可能起重要作用，并分析病毒感染是否在体外诱导鼻上皮细胞表达嗜酸性粒细胞趋化因子。

方法

取自鼻息肉切除术的鼻上皮细胞用甲型流感病毒（H3N2亚型）感染。在感染后8、24和48小时收集细胞和上清液。通过逆转录聚合酶链反应（RT-PCR）分析嗜酸性粒细胞趋化因子mRNA。通过酶联免疫吸附测定分析上清液中嗜酸性粒细胞趋化因子的浓度。我们还进行了阻断试验，以分析促炎细胞因子肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）对流感病毒诱导的嗜酸性粒细胞趋化因子产生的干预作用。